PubMed Health⌕ Search

Biomedical subjects

K Taki

Publications and source records attributed to K Taki.

At least 91 records · Page 5Linked to original sources
PubMed1988

The effects of SUN 1165, a novel sodium channel blocker, on ischemia-induced mitochondrial dysfunction and leakage of lysosomal enzymes in canine hearts.

The cardioprotective effect of SUN 1165, a novel sodium channel blocker, was investigated on ischemic myocardium. Nineteen anesthetized dogs were subjected to 2 hours coronary occlusion, and divided into 2 groups. In the control group, physiological saline was infused. In the SUN 1165 group, 2 mg/kg of SUN 1165 was injected intravenously. Two hours after occlusion, heart mitochondria were prepared from both ischemic and non-ischemic areas in each group, and their functions (RCI and St.III O2) were measured polarographically with succinate as a substrate. Fractionation of myocardial tissue from both non-ischemic and ischemic areas was performed according to the method of Weglicki et al., and the activities of lysosomal enzymes (NAG and beta-gluc) were measured. In the control group, mitochondrial dysfunction and leakage of lysosomal enzymes induced by 2 hours occlusion were observed. Administration of SUN 1165 maintained mitochondrial function, and prevented the leakage of lysosomal enzymes caused by ischemia significantly. These results indicated that SUN 1165 has a cardioprotective effect in ischemic heart.

Animals↗
PubMed1988

Differing time courses between delta lactate and mitochondrial respiration during coronary occlusion and after reperfusion in canine hearts.

The present study was designed to clarify whether or not a difference between arterial and venous lactate (delta lactate) levels is useful for evaluation of mitochondrial function in ischemia-reperfused myocardium. In the first experiment, 12 dogs were divided into 2 groups: 10-min occlusion of the left anterior descending coronary artery (LAD) followed by 10-min reperfusion, or 30-min occlusion followed by 40-min reperfusion, were performed. The lactate levels in the femoral artery and the great cardiac vein were measured enzymatically. delta Lactate was reversed immediately after occlusion. Ten min and 20 min were required for the recovery of delta lactate in the 10-min-occlusion with 10-min-reperfusion, and 30-min-occlusion with 40-min-reperfusion groups, respectively. In the second experiment, 36 dogs were divided into 6 groups: 10-min occlusion of LAD; 10-min occlusion with 10-min reperfusion; 30-min occlusion; and 30-min occlusion with 10-, 20-, or 40-min reperfusion were performed. Mitochondria from normal and occluded or reperfused areas were prepared, and the respiratory function of the mitochondria was measured polarographically. No significant decreases in the mitochondrial function were observed in the 10-min-occlusion, and 10-min-occlusion with 10-min-reperfusion groups. On the other hand, respiratory function of mitochondria was impaired by 30-min occlusion and was not improved by 10- or 20-min reperfusion. Significant recovery in the mitochondrial function was observed after 40-min reperfusion. That is, differing recovery time courses between delta lactate and the mitochondrial function were observed.

Animals↗
PubMed1988

Exchange of labeled bicarbonate and carbon dioxide with erythrocytes suspended in an elutriator.

An elutriator was used to study exchange of labeled CO2 and bicarbonate with erythrocytes. Rabbit erythrocytes were suspended by centrifugation in a stream of fluid and exposed to transient injections of an extracellular indicator (125I-albumin or 22Na+), a water indicator (3H2O), and H14CO3- and/or 14CO2. Diffusion of indicators into erythrocytes was judged by comparison of initial concentrations of diffusible and extracellular indicators in the elutriator outflow. It was possible to conduct these experiments at normal hematocrits because any carbonic anhydrase released from erythrocytes by hemolysis was washed away in the elutriator flow, and ambient pH, PO2, and PCO2 were kept constant by the inflow of fresh fluid. Equilibration of HCO3- with erythrocytes was complete during the 7- to 10-s transit time through the chamber. After this exchange was irreversibly inhibited by the anion exchange inhibitor, DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid), addition of carbonic anhydrase (100 mg/dl) accelerated exchange, but acetazolamide (20 mg/dl) was without effect. These observations were consistent with the absence of carbonic anhydrase on the surface of the erythrocytes.

Animals↗
PubMed1988

Existence of leukotoxin 9,10-epoxy-12-octadecenoate in lung lavages from rats breathing pure oxygen and from patients with the adult respiratory distress syndrome.

Pulmonary influxed neutrophils have been suggested to be involved in the development of hyperoxia-induced lung injury. We recently revealed that a highly toxic substance, 9,10-epoxy-12-octadecenoate, is biosynthesized by human neutrophils, thus it was named leukotoxin. Because hyperoxia-induced lung injury is a model of adult respiratory distress syndrome (ARDS), this study was designed to investigate whether or not leukotoxin is involved in the genesis of pulmonary oxygen toxicity and ARDS. After exposure to hyperoxia for 60 h, rats showed acute pulmonary edema, which was evidenced by increased lung weight, albumin concentrations, and angiotensin-converting enzyme (ACE) activities in lung lavages. These changes were correlated with an increased number of neutrophils. We detected leukotoxin in lung lavages of rats after exposure to hyperoxia for 60 h by high performance liquid chromatography and gas-chromatography/mass spectrometry. After intravenous injection of leukotoxin (100 mumol/kg) to rats, acute edematous lung injury occurred showing increases in lung weight, lung lavage albumin concentrations, and lung lavage ACE activities. In the lung lavages obtained from 5 patients with ARDS, significant increases in albumin concentrations and ACE activities were observed compared with those from subjects without pulmonary disease. Moreover, considerable amounts of leukotoxin, 38.5 +/- 21.9 nmol/lung lavage, were observed in the lavages from patients with ARDS. These findings suggest that leukotoxin plays an important role in the genesis of acute edematous lung damage in pulmonary oxygen toxicity, and that leukotoxin also links with the development of lung injury observed in patients with ARDS.

Animals↗
PubMed1988

Effects of isosorbide dinitrate on thromboxane A2 synthesis in carbon dioxide exposed platelets.

Isosorbide dinitrate (Nitorol R, 100 nmol/l) blocked an increase in thromboxane B2 concentration in human platelet-rich plasma caused by exposure to high CO2 tension, in the presence of arachidonic acid. Thromboxane B2 concentrations obtained at 1 or 2 mmol/l or arachidonic acid were not influenced by isosorbide dinitrate at low CO2 tension. Inhibitory action of isosorbide dinitrate on the thromboxane A2 synthesis appears to have a close relation to the site of CO2 action.

Blood Platelets↗
PubMed1987

Lysozyme activity of cystic mucosal and submucosal glands in the stomal area of the gastric remnant.

In order to study the lysozyme activity in the cystic mucosal and submucosal glands in the stomal area of the gastric remnant, which is one of the components of gastritis cystica polyposa, we carried out a pathological and immunohistochemical examination of 55 patients with gastric remnants, including 19 with stomal carcinoma, after partial gastrectomy for benign gastro-duodenal diseases. These stomach specimens were examined immunohistochemically for lysozyme. The cytoplasm of some epithelial cells of cystic mucosal and submucosal glands, which showed characteristic changes in the gastro-intestinal stoma as well as background changes in the stomal carcinoma, showed a strongly positive reaction for lysozyme. These strongly lysozyme-positive cells in the cystic mucosal glands appeared more frequently in the cases of stomal carcinoma than in the non-cancerous controls.

Aged↗
PubMed1987

Graphic analysis of serotonin effects in dog heart-lung preparation.

Graphical analysis of the effects of serotonin on cardiac function and pulmonary circulation was performed, using the dog heart-lung preparation. The equilibrium points, at which the cardiac output (CO)-curve and venous return (VR)-curve cross in the right atrial pressure (RAP) or left atrial pressure (LAP)-CO relations, were directly recorded on two X-Y recorders. CO- and VR-curves were directly depicted by changing the blood level in the reservoir, and by inducing ventricular fibrillation and simultaneously occluding pulmonary arterial trunk, respectively. Single injections of serotonin, 300 micrograms, into the right or left atrium, induced a negative inotropic response. Low rate (less than 30 micrograms/min) of infusion of serotonin had no effect on the CO-curve or on the slope-gradient of VR-curve in the LAP-CO relation. At a rate of 60 or 120 micrograms/min, however, the CO-curve was moved downwards to the right, indicating a negative inotropic effect. Pulmonary mean filling pressure increased and the slope-gradient of pulmonary VR-curve decreased, indicating an increased resistance to venous return from the pulmonary circulation. Pulmonary arterial pressure was markedly elevated. In order to obtain the capacitance ratio between the extracorporeal circuit and the pulmonary circulation, a shift of blood volume to the pulmonary circulation was induced by elevating the aortic pressure, which also decreased the slope-gradient. The calculated capacitance ratio became greater during the infusion of serotonin, indicating that the capacitance in the pulmonary circulation was lowered. It is likely that serotonin has contractile effects on the pulmonary arterial and venous vascular beds, elevating the pulmonary filling pressure and resistance to venous return.

Animals↗
PubMed1987

Management of acid-base balance with red blood cell carbonic anhydrase (RCA). II. Control of acid-base balance with acetazolamide.

Acetazolamide, a carbonic anhydrase (CA) inhibitor, was used to normalize metabolic alkalemia. A dosage of acetazolamide for normalizing metabolic alkalemia has not yet been experimentally determined. The dosage of acetazolamide for this purpose is experimentally calculated in this paper. The correlation between various concentration of acetazolamide mixed with blood and the base excess (BE) levels in blood at the start of normalizing metabolic alkalosis was studied in vitro. The change rate of the BE level was calculated from BE levels noted before and after tonometry of the blood with and without acetazolamide. A dosage of acetazolamide which can cause the change rate of the BE level to decrease is considered to be an effective dosage. Metabolic alkalosis in vitro was produced by adding bicarbonate into the blood. An effective dosage of acetazolamide for metabolic alkalemia of which the BE range was from 0 to + 30 mEq/liter was calculated. CA activities in the kidney and the blood of dogs administered acetazolamide were examined. The effective dosage of acetazolamide obtained from in vitro experiments inhibited the CA activities not only in the blood but also in the kidneys. An effective dosage of acetazolamide to normalize a BE of + 10 mEq/liter in vitro was converted into about 7-12 mg/kg in vivo. This dosage inhibited the red blood cell carbonic anhydrase (RCA) activity to 20-40%, whereas the normal physiological variation range is 25%. An effective dosage of acetazolamide in the blood did not proportionally increase with an increase of HCO3- during severe alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1987

In vivo localization of radiolabeled monoclonal antibody to carcinoembryonic antigen (CEA) in a CEA-producing tumor--comparison with polyclonal antibody.

To compare accumulation of the 125I-labeled antibodies (anti-carcinoembryonic antigen (CEA) monoclonal antibody and polyclonal antibody) to a CEA-producing tumor (SC-2-JCK), an in vivo localization study was performed in nude mice. The tumor-to-blood ratio at 120 hours after injection rose to 4.6 for the monoclonal antibody, but remained at 1.3 for the polyclonal antibody. However, no differences were noted between the antibodies up to 72 hours after injection. In autoradiograms, selective accumulation of the tracer was noted in the tumor for both antibodies. However, no superiority or inferiority of imaging for either of the antibodies could be definitely determined.

Adenocarcinoma, Papillary↗
PubMed1986

Plasma-free eicosapentaenoic acid/arachidonic acid ratio: a possible new coronary risk factor.

Seventy-six effort angina patients who had typical angina on exertion documented by treadmill stress test with evidence of ischemic ST-segment depression and 78 healthy volunteers in urban Japan were investigated in this study. Plasma free fatty acids (FFA) in both groups were determined using high-performance liquid chromatography. The relationships between the total cholesterol, high-density lipoprotein (HDL), triglycerides in plasma, and the genesis of coronary heart disease were also examined. The ratio (0.08 +/- 0.08) of eicosapentaenoic acid (EPA)/arachidonic acid (AA) in plasma FFA was significantly lower in effort angina patients than that (0.15 +/- 0.12) in healthy volunteers. The lower ratio was due to significantly lower levels of EPA in the patients than in normals. In 42% of angina patients, the ratio is below 0.03. In all age subgroups except the age 30-39 subgroup, the ratio of EPA/AA was significantly lower in patients than in normals, when divided into four subgroups by using a 10-year age interval. Though the total cholesterol and triglycerides were not significantly different between the two groups, HDL was significantly lower and total cholesterol/HDL ratio was significantly higher in effort angina patients than in healthy volunteers. However, there was no correlation between EPA/AA ratio and HDL in individuals in either group. From these results, it could be concluded that lower EPA/AA ratio is a new coronary risk indicator other than HDL.

Adult↗
PubMed1986

Syntheses of selenium labelled compounds--II. The exchange reaction with elemental selenium.

73Se labelled 2-selenouracil was prepared by the isotope exchange reaction method. It has been well known that in order to prepare labelled compounds in high specific activity by exchange reaction, the substrate compounds have to be used in small quantities. For 2-selenouracil, however, the reaction in low concentration is not always preferable for the labelling of high specific activity within a limited time. The optimum conditions for the preparation of [2-73Se]-2-selenouracil of maximum specific activity were determined.

Humans↗
PubMed1986

Reliability in determination of methanol concentration.

Two sampling methods for reliable determination of methanol concentration were studied. Methanol vapor stored in glass container was found to be decomposed on the glass surface. The decomposition increased as the surface area of the glass container was extended. The proportion of the decomposition in the glass container was relatively high, especially when the concentration of methanol vapor was low. Therefore, a reliable determination by the above sampling method was impossible. In the solid sorbent sampling by silica gel, the collected methanol was also decomposed, but the decomposed amount was negligibly small compared to the collected methanol when the amount of methanol was more than 0.1 microliter of the liquid methanol. It could be concluded from the foregoing findings that the determination of methanol concentration by this method is reliable.

Air Pollutants, Occupational↗
PubMed1986

Disturbance of CO2 elimination in the lungs by carbonic anhydrase inhibition.

Carbonic anhydrase in the red blood cell and in the pulmonary endothelium facilitates the elimination of CO2 in the lungs. Although a carbonic anhydrase inhibitor, such as acetazolamide which is frequently used in patients with glaucoma or with metabolic alkalosis, is known to impair the CO2 elimination in the lungs, the dose-response curve of CO2 elimination with acetazolamide has not been well documented in CO2 homeostasis. In the present study, the effects of inhibited carbonic anhydrase were tested in 8 anesthetized dogs; various dosages of acetazolamide were used. When the administered clinical dosage of acetazolamide increased from 5 to 20 mg/kg, PaCO2, PVCO2, arterial-alveolar PCO2 difference (a-ADCO2), and physiological VD/VT ratio increased progressively to 52.0 +/- 2.1 Torr, 58.0 +/- 3.0 Torr, 23.4 +/- 1.2 Torr, and by 19.2 +/- 1.8% (S.E.) respectively, whereas inhibition rate of red blood cell carbonic anhydrase (RCA) activity increased progressively to 73.1 +/- 2.1% (S.E.). On the other hand, PACO2 decreased to 27.1 +/- 1.8 Torr (S.E.) upon the first injection of 5 mg/kg of acetazolamide, but PACO2 did not change further upon 3 additional 5 mg/kg injections. Mixed venous-arterial PCO2 difference [V-a)PCO2), VCO2, and anatomical VD/VT ratio were unchanged by the administration of any doses of acetazolamide.

Acetazolamide↗
PubMed1986

[Electrocardiographic alterations in expired cases due to ruptured cerebral aneurysm: correlation with other complications relating to the autonomic nervous system].

Forty three expired cases due to ruptured cerebral aneurysm were studied in electrocardiographic alterations with special reference to other complications of the autonomic nervous system. The cases with past history of ischemic cardiovascular disease had been excluded. The age of the patients ranged between 23 to 79 years old (average 50.1 years old). The clinical condition of the patients according to Hunt & Kosnik classification I in 1 case, II in 11 cases, III in 14 cases, and IV & V in 17 cases. The duration between the aneurysm rupture and admission was within 24 hours in 16 cases, 2 to 3 days in 13 cases, 4 to 7 days in 9 cases, and 2 to 3 weeks in 5 cases. The site of ruptured aneurysms was anterior communicating artery in 12 cases, internal carotid artery in 24 cases, and others in 7 cases. The direct surgeries to the aneurysms were performed in 22 cases, and not done in 21 cases. The electrocardiographic alterations were found as follows: flat or inverted T in 19 cases, prolonged QTc in 33 cases, manifest U in 14 cases, ST elevation or depression in 10 cases, Ta (atrial T) in 10 cases, left ventricular hypertrophy in 8 cases, sinus tachycardia in 7 cases, sinus bradycardia in 12 cases, and arrhythmias with SVPC or VPC (supraventricular or ventricular premature contraction), or sinus arrhythmia in 12 cases. Prolonged QTc, and flat or inverted T were most often found in the cases with ruptured aneurysm of the anterior communicating artery, and next in those with the internal carotid artery, and least often in those with others.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Cerebral blood flow during open-chest cardiac massage with occlusion of the descending aorta in dogs.

Cerebral blood flow (CBF) and carotid blood flow (CAF) during open-chest cardiac massage with and without occlusion of the descending aorta was examined in 10 dogs to assess whether they were augmented by occlusion. In control measurements with a normally beating heart, CBF with and without occlusion of the descending aorta were 17.8 +/- 2.3 and 13.8 +/- 2.2 ml/min (+/- S.E.M.), which were not significantly different. Cerebral blood flow during open-chest cardiac massage were 6.1 +/- 1.0 with occlusion and 5.7 +/- 1.0 ml/min without occlusion of the descending aorta, which were also not significantly different. By contrast, CAF increased significantly with occlusion of the descending aorta both during control measurement, with mean increases of 61.1% and 92.2% during open-chest cardiac massage (P = 0.05). While occlusion generally failed to augment CBF; in two dogs resuscitation was successful by manual cardiac massage. With the restoration of cardiac activity it increased immediately to twice that of control blood flow, and then gradually returned to the control level. Based on these observations, it is the author's opinion that every effort should be directed toward the restoration of cardiac activity as quickly as possible during circulatory arrest, and to increase CBF which is essential for neurological recovery.

Animals↗
PubMed1985

[Circulating negative inotropic substance produced by the lung, affected by prostaglandin and thromboxane].

The Lung is capable of the synthesis and the release of prostaglandins responded to a number of pathophysiological stimuli, which may impair myocardial performance. Present study was undertaken to determine the release of circulating negative inotropic substance(s) from the lung and whether or not blockage of prostanoid synthesis, or infusion of prostaglandin are related to the production of this substance(s). Sixteen isolated left lower lobes were divided into 3 groups: (1) untreated, isolated blood-perfused lungs (n = 5), (2) prostaglandin I2, 1 microgram/min, continuously added to the perfusate (n = 6), and (3) five lobes pretreated with ibuprofen (12.5 mg/kg) in addition to 1 microgram/min prostaglandin I2. Perfusion of an isolated lobe with heparinized whole blood caused thrombocytopenia. The plasma 4 hours after perfusion led to the generation of a humoral agent(s) that reduced developed tension (Tpd) of a papillary muscle (p less than 0.05), and Ca++ -and Mg++-ATPase of sarcoplasmic reticulum (SR) (p less than 0.01). With prostaglandin I2, thromboxane B2 rose from 0.076 to 0.362 ng/ml at a level higher than control (p less than 0.05). The plasma significantly lowered SR-ATPase and myofibril-Mg++-ATPase activities and further reduced papillary muscle Tpd. By pretreatment with ibuprofen, adverse prostaglandin I2 effects were eliminated. The observation suggests that the lung produces prostaglandin related negative inotropic substance(s) that may reduced contractility, affected by energy availability.

Adenosine Triphosphatases↗